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Circulation. 2007;116:e92
doi: 10.1161/CIRCULATIONAHA.107.697540
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(Circulation. 2007;116:e92.)
© 2007 American Heart Association, Inc.


Correspondence

Letter by O’Rourke Regarding Articles, "Prevalence of Long-QT Syndrome Gene Variants in Sudden Infant Death Syndrome," "Cardiac Sodium Channel Dysfunction in Sudden Infant Death Syndrome," and "Contribution of Long-QT Syndrome Genes to Sudden Infant Death Syndrome: Is It Time to Consider Newborn Electrocardiographic Screening?"

Michael F. O’Rourke, MD, DSc

St. Vincent’s Clinic, University of New South Wales, Sydney, Australia

To the Editor:

I read with interest the papers by Arnestad et al1 and Wang et al,2 as well as the editorial by Berul and Perry,3 which rekindle debate on neonatal assessment of long-QT syndrome as an underlying cause of sudden infant death syndrome. The authors appear to presume that ventricular fibrillation (VF) is responsible for the lethal event, and they liken this to sudden death in adults with ischemic and other cardiac disease.

As supervisor of cardiac activities in the ambulance service for the Australian state of New South Wales (population, 6.3 million), I had the opportunity to review 12 490 cases of sudden cardiac arrest in which ECG monitoring was performed with defibrillator pads or paddles.4 VF was the original rhythm in 40% of adults, but in <5% of young children. Hospital survival for VF in adults was {approx}13% but zero for infants over the 10-year period.

Our findings provide no enthusiasm for mass ECG or genetic screening, or for focus on tachyarrhythmia with consideration of ß-blocker therapy or defibrillator implant. Findings do support the majority view that a respiratory event is the primary cause of most sudden infant death syndrome cases. Attention to respiratory issues (ie, position in crib, location of pillow and bedclothes, passive smoking) have led to a dramatic fall in the occurrence of sudden infant death syndrome in Australia.5

Before health authorities promote any screening or treatment plan aimed at prevention of VF in infants, it is desirable that they first question their assumptions and provide evidence that infantile VF is a correctable problem in society.


*    Acknowledgments
 
Disclosures

None.


*    References
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*References
 

  1. Arnestad M, Crotti L, Rognum TO, Insolia R, Pedrazzini M, Ferrandi C, Vege A, Wang DW, Rhodes TE, George AL Jr, Schwartz PJ. Prevalence of long-QT syndrome gene variants in sudden infant death syndrome. Circulation. 2007; 115: 361–367.[Abstract/Free Full Text]
  2. Wang DW, Desai RR, Crotti L, Arnestad M, Insolia R, Pedrazzini M, Ferrandi C, Vege A, Rognum T, Schwartz PJ, George AL Jr. Cardiac sodium channel dysfunction in sudden infant death syndrome. Circulation. 2007; 115: 368–376.[Abstract/Free Full Text]
  3. Berul C, Perry J. Contribution of long-QT syndrome genes to sudden infant death syndrome: is it time to consider newborn electrocardiographic screening? Circulation. 2007; 115: 294–296.[Free Full Text]
  4. Adelstein BA, O’Rourke MF, Love A. Out-of-hospital VF in children: frequency and outcome. Circulation. 1998; 98 (suppl 1): I-140.
  5. Dwyer T, Ponsonby AL. The decline of SIDs: a success story of epidemiology. Epidemiology. 1996; 7: 323–325.[Medline] [Order article via Infotrieve]

Related Article:

Issue Highlights
Circulation 2007 116: 359. [Full Text]




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Right arrow Articles by O’Rourke, M. F.
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PubMed
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Right arrow Articles by O’Rourke, M. F.
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Medline Plus Health Information
*Genetic Testing
*Sudden Infant Death Syndrome
Related Collections
Right arrow CPR and emergency cardiac care
Right arrow Pediatric and congenital heart disease, including cardiovascular surgery
Right arrowRelated Article